Verticillium dahliae CFEM Effector VdCR Stabilises the Susceptibility Factor GhAGP31 to Suppress Host Vascular Immunity and Promote Cotton Verticillium Wilt

Plant pathogenic fungi secrete a wide array of effector proteins to manipulate host immunity, including those containing CFEM (Common in Fungal Extracellular Membranes) domains. Here, we identified a CFEM domain-containing effector VdCR from Verticillium dahliae, the causal agent of cotton Verticillium wilt. The expression of VdCR was drastically upregulated during cotton infection. Targeted deletion of VdCR compromised fungal oxidative stress resistance and pathogenicity on cotton, establishing it as a key virulence factor. VdCR physically targets cotton non-classical arabinogalactan protein GhAGP31 via its CFEM domain. Virus-induced gene silencing (VIGS) of GhAGP31 significantly enhanced reactive oxygen species (ROS) accumulation, callose and lignin deposition, and plant resistance to V. dahliae, confirming that GhAGP31 acts as a negative regulator of vascular immunity. In addition, we identified GhAGP31 as a negative regulator of cotton vascular development, revealing its dual roles in coordinating plant immunity and development. We further verified that VdCR stabilises GhAGP31 to promote its accumulation both in vitro and in planta. Collectively, this study demonstrates that GhAGP31 functions as a novel cotton susceptibility factor that suppresses both vascular immunity and development and can be stabilised by the V. dahliae CFEM effector VdCR to facilitate fungal infection.